PMID- 23991758
OWN - NLM
STAT- MEDLINE
DCOM- 20140620
LR  - 20131015
IS  - 1525-6049 (Electronic)
IS  - 0886-022X (Linking)
VI  - 35
IP  - 10
DP  - 2013
TI  - Efficacy of antisense monocyte chemoattractant protein-1 (MCP-1) in a rat model 
      of mesangial proliferative glomerulonephritis.
PG  - 1418-28
LID - 10.3109/0886022X.2013.828309 [doi]
AB  - OBJECTIVE: The effects of inhibition of monocyte chemoattractant protein-1 
      (MCP-1) on a rat model of mesangial proliferative glomerulonephritis (MsPGN) were 
      evaluated. METHODS: The anti-Thy-1 MsPGN model was developed by intravenously 
      injecting anti-Thy-1 monoclonal antibodies into rats, followed by an injection of 
      mesangial cells transfected with antisense MCP-1 into the renal artery. Exogenous 
      cells were detected by in situ hybridization. Rats (40 total) were randomly 
      divided into five groups: SO (sham operation), TG (Thy-1 glomerulonephritis 
      model), MC (non-transfected normal rat mesangial cell), BC (pLXSN empty vector or 
      blank control), and AM (antisense MCP-1 transfection) groups. Effects of 
      exogenous MCP-1 on urinary protein excretion rate, biochemical parameters, and 
      pathological changes were evaluated. Expression of MCP-1 and transforming growth 
      factor-beta1 (TGF-beta1) were detected by immunohistochemistry. mRNA expression of 
      MCP-1, TGF-beta1, and CC chemokine receptor 2 (CCR2) were detected by RT-PCR. 
      RESULTS: Exogenous MCP-1 cDNA was successfully transfected into mesangial cells. 
      Exogenous mesangial cells were detected in glomeruli by in situ hybridization. 
      Glomerular mesangial cell proliferation, 24-h urinary protein excretion rate, 
      mRNA expression of MCP-1, TGF-beta1, and CCR2, and protein expression of MCP-1 all 
      decreased in the AM group as compared to the control group (p < 0.05), but there 
      was no significant difference in the expression level of TGF-beta1 protein. 
      CONCLUSIONS: (1) Mesangial cells can be used as a vector to transfect exogenous 
      genes into kidneys; (2) antisense MCP-1 decreases mesangial cell proliferation 
      and pathological injury in MsPGN model rats by decreasing expression of MCP-1 and 
      CCR2; and (3) antisense MCP-1 suppressed mesangial cell proliferation and matrix 
      accumulation in anti-Thy-1 MsPGN model rats, which did not entirely depend on 
      TGF-beta1.
FAU - Liu, Hua
AU  - Liu H
AD  - Division of Pediatric Nephrology, The Children's Medical Center, The Second 
      Xiangya Hospital, Central South University , Changsha , China and.
FAU - Zhang, Xin-Ping
AU  - Zhang XP
FAU - Yi, Zhu-Wen
AU  - Yi ZW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130902
PL  - England
TA  - Ren Fail
JT  - Renal failure
JID - 8701128
RN  - 0 (Ccr2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA, Antisense)
RN  - 0 (Isoantibodies)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Tgfb1 protein, rat)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (anti-Thy antibody)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/*antagonists & inhibitors/metabolism
MH  - DNA, Antisense/*therapeutic use
MH  - Disease Models, Animal
MH  - Female
MH  - Genetic Therapy
MH  - Glomerulonephritis, Membranoproliferative/*drug therapy
MH  - Isoantibodies
MH  - Mesangial Cells/metabolism
MH  - Proteinuria/drug therapy
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, CCR2/metabolism
MH  - Transforming Growth Factor beta1/metabolism
EDAT- 2013/09/03 06:00
MHDA- 2014/06/21 06:00
CRDT- 2013/09/03 06:00
PHST- 2013/09/03 06:00 [entrez]
PHST- 2013/09/03 06:00 [pubmed]
PHST- 2014/06/21 06:00 [medline]
AID - 10.3109/0886022X.2013.828309 [doi]
PST - ppublish
SO  - Ren Fail. 2013;35(10):1418-28. doi: 10.3109/0886022X.2013.828309. Epub 2013 Sep 
      2.